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Congenital Cytomegalovirus and HIV Perinatal Transmission

Adachi, Kristina, MD*; Xu, Jiahong, MS, MPH; Ank, Bonnie, BA*; Watts, D. Heather, MD; Camarca, Margaret, RN, MPH; Mofenson, Lynne M., MD§; Pilotto, Jose Henrique, MD; Joao, Esau, MD; Gray, Glenda, MD**; Theron, Gerhard, MD††; Santos, Breno, MD‡‡; Fonseca, Rosana, MD§§; Kreitchmann, Regis, MD¶¶; Pinto, Jorge, MD‖‖; Mussi-Pinhata, Marisa M., MD***; Machado, Daisy Maria, MD†††; Ceriotto, Mariana, MD‡‡‡; Morgado, Mariza G., PhD§§§; Bryson, Yvonne J., MD*; Veloso, Valdilea G., MD§§§; Grinsztejn, Beatriz, MD, PhD§§§; Mirochnick, Mark, MD¶¶¶; Moye, Jack, MD§; Nielsen-Saines, Karin, MD* MPH for the NICHD HPTN 040 Study Team

The Pediatric Infectious Disease Journal: October 2018 - Volume 37 - Issue 10 - p 1016–1021
doi: 10.1097/INF.0000000000001975
Maternal-Neonatal Reports
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Background: Congenital cytomegalovirus (CMV) infection (cCMV) is an important cause of hearing loss and cognitive impairment. Prior studies suggest that HIV-exposed children are at higher risk of acquiring cCMV. We assessed the presence, magnitude and risk factors associated with cCMV among infants born to HIV-infected women, who were not receiving antiretrovirals during pregnancy.

Methods: cCMV and urinary CMV load were determined in a cohort of infants born to HIV-infected women not receiving antiretrovirals during pregnancy. Neonatal urines obtained at birth were tested for CMV DNA by qualitative and reflex quantitative real-time polymerase chain reaction.

Results: Urine specimens were available for 992 (58.9%) of 1684 infants; 64 (6.5%) were CMV-positive. Mean CMV load (VL) was 470,276 copies/ml (range: < 200–2,000,000 copies/ml). Among 89 HIV-infected infants, 16 (18%) had cCMV versus 42 (4.9%) of 858 HIV-exposed, uninfected infants (P < 0.0001). cCMV was present in 23.2% of infants with in utero and 9.1% infants with intrapartum HIV infection (P < 0.0001). Rates of cCMV among HIV-infected infants were 4-fold greater (adjusted OR, 4.4; 95% CI: 2.3–8.2) and 6-fold greater among HIV in utero–infected infants (adjusted OR, 6; 95% CI: 3–12.1) compared with HIV-exposed, uninfected infants. cCMV was not associated with mode of delivery, gestational age, Apgar scores, 6-month infant mortality, maternal age, race/ethnicity, HIV viral load or CD4 count. Primary cCMV risk factors included infant HIV-infection, particularly in utero infection.

Conclusion: High rates of cCMV with high urinary CMV VL were observed in HIV-exposed infants. In utero HIV infection appears to be a major risk factor for cCMV in infants whose mothers have not received combination antiretroviral therapy in pregnancy.

From the *David Geffen UCLA School of Medicine, Los Angeles, CA

Westat, Rockville, MD

Office of the Global AIDS Coordinator, U.S. Department of State, Washington, DC

§Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD

Hospital Geral de Nova Iguaçu, Nova Iguaçu, RJ, Brazil

Hospital Federal dos Servidores do Estado, Rio de Janeiro, RJ, Brazil

**SAMRC and Perinatal HIV Research Unit, University of Witwatersrand, Cape Town, South Africa

††Stellenbosch University/Tygerberg Hospital, Cape Town, South Africa

‡‡Hospital Conceicao, Porto Alegre, RS, Brazil

‡‡Hospital Femina, Porto Alegre, RS, Brazil

¶¶Irmandade da Santa Casa de Misericordia de Porto Alegre, RS, Brazil

‖‖Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

***Ribeirão Preto Medical School, University of São Paulo, SP, Brazil

†††Escola Paulista de Medicina-Universidade Federal de São Paulo, São Paulo, SP, Brazil

‡‡‡Foundation for Maternal and Infant Health (FUNDASAMIN), Buenos Aires, Argentina

§§§Fundacao Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, RJ, Brazil

¶¶¶Boston University School of Medicine, Boston, MA.

Accepted for publication November 13, 2017.

Clinical Trials Registration: NCT00099359.

The content, conclusions and opinions expressed in this article are those of the authors and do not necessarily represent those of the National Institutes of Health, the U.S. Department of Health and Human Services or the U.S. Department of State, affiliated universities, programs or companies.

Change of Author Affiliations: Lynne Mofenson, MD, has retired from service at the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, but is currently working with the Elizabeth Glaser Pediatric AIDS Foundation, Washington, DC. D. Heather Watts was previously at the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, but is currently at the Office of the Global AIDS Coordinator, U.S. Department of State, Washington D.C.

The NICHD HPTN 040 study was supported by NICHD Contract # HHSN267200800001C (NICHD Control # N01-HD-8-0001) and U01 AI047986 (Brazilian AIDS Prevention Trials International Network), NIAID/ NIH. Overall support for the International Maternal Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT) was provided by the National Institute of Allergy and Infectious Diseases (NIAID) U01 AI068632, UM1AI068632 (IMPAACT LOC), UM1AI068616 (IMPAACT SDMC) and UM1AI106716 (IMPAACT LC), with co-funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health (NIMH) AI068632. The original parent study was supported in part by Boehringer Ingelheim Pharmaceuticals Inc. and GlaxoSmithKline, on behalf of ViiV Healthcare. Support was also provided by the UCLA Children’s Discovery and Innovation Institute through the Harry Winston Fellowship Award, the UCLA AIDS Institute, the UCLA Center for AIDS Research (CFAR) NIH/ NIAID AI02869 and AI28697, and the UCLA Pediatric AIDS Coalition.

The authors have no funding or conflicts of interest to disclose.

Prior Presentations: Nielsen-Saines K for the NICHD HPTN 040 Study Team. Increased CMV Co-Infection with In Utero-Acquired HIV-1. Oral abstract 2695.8. 2013 Pediatric Academic Society Meetings. Washington, D.C., May 4–7, 2013.

Address for correspondence: Kristina Adachi, MD, Department of Pediatrics, Division of Infectious Diseases, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave, MDCC 22–442, Los Angeles, CA 90095–1752. E-mail: kadachi@mednet.ucla.edu.

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